Body Systems: Circulatory System Flashcards
main function of circulatory system
transport of oxygen, nutrients, waste products and hormones among the tissues and organs of the body
circulatory system
heart, blood vessels, blood
heart
4 chambers:
- right atrium
- left atrium
- right ventricle
- left ventricle
atria
collect blood from the body and lungs and pass it to the ventricles
ventricles
eject blood throughout the body
myocardium
chamber walls consisting of cardiac muscle
- internal lining consists of a smooth membrane called endocardium
pericardium
double-layered membrane that encloses the heart
atrioventricular (AV) valves
permit one-way blood flow form the atria to the ventricles
tricuspid valve
three flaps (cusps) that meet when valve is closed between the right atrium and right ventricle
pumping cycle
chamber relax as they fill and the contract when the pump blood
- diastole: filling period
- systole: contracting period
- alternation contraction and filling called cardia cycle
sinoatrial node (SA node)
pacemaker of the heart
- initiates impulse for contraction thats spreads over atria and passes to the ventricles via conductive tissue called the atrioventricular node (AV node)
- impulse continues along and terminate in the Purkinje fibres
heart muscle contraction influenced by
autonomic nervous system and hormones such as epinephrine
sets of nerves
two sets work with one slowing the heart and the other accelerating it
- vagus nerve: slows heart rate during rest ad sleep by acetylcholine
aorta
branches carry blood to head, chest, abdomen, pelvis, and lower extremities
- arteries divide into smaller arteries and eventually into arterioles, which then lead into capillaries
- walls of arteries are muscular, thick, strong, elastic, and lined with endothelium
red blood cells (erythrocytes)
- make up half of the blood’s volume
- most abundant cells in the human body
- mature red blood cells have no nucleus
- carrying protein called hemoglobin
- short lifespan due to lack of nucleus
hemoglobin
- made up of protein called gloving and iron-containing heme molecule
- most important component of RBC
- in lungs, hemoglobin binds to o2 becoming oxyhemoglobin
plasma
- consists of mostly water carrying nutrients, wastes, ions, hormones, clotting factors, albumins, and antibodies
- clotting factors readily available, and antibodies to address any infection in body
- albumin promotes blood’s ability to hold water and maintain pressure inside blood vessels
white blood cells (leukocytes)
- produced in the bone marrow from their respective system
- primary function is to defend tissues against infections and foreign substances
- abnormalities an defects in the WBCs can result in disease and disability
platelets
- produced in bone marrow and essential for blood clotting
- clotting factors formed in the liver, enter the blood and become active in response to an injury
- during clotting formation, platelets become sticky and release a protein called fibrin which forms a dense mash at the wound, preventing blood loss
blood tests
diagnostic for systemic diseases and specific blood disorders
- measure total blood count (RBC + WBC + platelets) and other components within blood
- provides qualitative information including size, shape, and ratio
bone marrow smear
used to diagnose malignant blood disorders and increases or decreases in blood counts
- provide information on the function of the bone marrow an the qualitative characteristics of stem cells that create blood cells
electrocardiogram
electrical recording of heart action aiding in the diagnosis of coronary artery disease, myocardial infarction, valve disorders, and some congenital heart disease
echocardiography
high-frequency sound waves utilized to examine size, shape, and motion of hear structured
doppler echocardiography
explores blood flow patterns and changes in velocity of blood flow within the heart and great vessels
cardia catheterization
catheter passed into heart through blood vessels to Samp.e the blood in each chamber for O2 content and pressure
coronary arteriography
injecting a contract material to visualize blood vessel function
arrhythmias/dysrhythmias
irregular cardiac
- tachycradia: too fast
- bradycardia: too slow
cardiovascular disease
- almost 1/3 of deaths in western countries attributed to heart disease –> most by coronary artery disease and hypertension
- important ss: chest pain, dyspnea, tachypnea, palpitations. cyanosis, edema, fatigue, syncope
hyperlipidemia
- elevated lipids blood like cholesterol, phospholipids, and triglycerides
- cholesterol is transported throughout by transport protein called lipoproteins
hyperlipidemia low-density lipoprotein
- LDL
- major cholesterol carrier in blood
- accumulation of LDL can form a plaque (thick, heard deposit( that narrows arteries impeding blood flow
as blood LDL increases the risk for heart disease increases - estimated 35% of adults over 20 have high levels of LD
hyperlipidemia high density lipoprotein
- HDL
- carries 1/4 to 1/3 of the cholesterol
- generally, the higher the level of HDL, the lower the risk of coronary heart disease (CAD)
coronary artery disease (CAD)
involves arteries supplying myocardium
CAD ss
- asymptomatic inutialy
- first symptom is pain of angina pectoris
- advanced: burning, squeezing, crushing, radiating to arm/neck/jaw pain
- nausea, vomiting, weakness
CAD prognosis
- depends on response to treatment
- stop smoking
CAD diagnosis
- changes in ECG but not always recognized, can show ischaemia and arrhythmias as well
- treadmill testing
- thallium or cardiolite scan
- CT scan
- stress echocardiogram
- angiogram
- cardiac catherization
CAD treatment
- restore good blood blow to myocardium - use vasodilators
- angioplasty with a balloon or stent attempted to open constricted arteries
- reduction of plaque buildup with hypolipidemic drugs
- angiotensin converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics
- anticoagulants to prevent blood clots breaking off
- coronary artery bypass surgery if no response to drugs and angioplasty
- experimental gene therapy injecting DNA into cardia muscle to stimulate growth of new cells
CAD etiology
- deposits o fat containing plaque in the lumen of coronary arteries results in arteriosclerosis and subsequent narrowing of the lumen of the arteries causing temporary cardia ischaemia and eventually MI
- pain due to diminished blood flow and low O2 saturation
- screening important because it can be asymptomatic until a sudden death or Mi
- myocardium needs adequate blood flow to function, without enough it dies
- arteriosclerosis: hardening of the arteries so that they lose elasticity and become hard and narrow leading to cardia ischaemia
- pain not usually experienced until 75% of coronary artery is blocked
- high risk: genetic predisposition, men older than 40, post-menopausal women, caucasians, smoking, urban society residents, hypertension, diabetes, obesity, elevated cholesterol, lack of exercise, stress
CAD prevention
- diet low in fat, salt, cholesterol
- exercise
- reduce stress and smoke
angina pectoris
reduced oxygen supplied to myocardium leading to chest pain
angina pectoris ss
- sudden onset of left sided chest pain during or after exertion
- pain my radiate to left arm/back
- dyspnea, hypertension, arrhythmias
angina pectoris etiology
- atherosclerosis causes narrowing of coronary arteries, compromising blood flow to myocardium
- exercise requires increased blood flow, but vessels cannot supply it
- causes: spasms of coronary arteries, severe tachycardia, anemia, respiratory disease
angina pectoris prognosis
- depends on extent of arterial involvement
- lower strenuous activities and vasodilators can cause angina pectoris to diminish or disappear
- modify lifestyle
angina pectoris diagnosis
- ECG showing ischaemia
- similar diagnostic measures as for CAD
angina pectoris treatment
- cease strenuous activity
- nitroglycerin tablets or spray
angina pectoris prevention
- lifestyle modification
- site low in fat, cholesterol, and salt
- control of hypertension
- weight loos
- smoking cessation
- reduce stress
myocardial infarction (MI)
death of myocardial tissue caused by development of ischemia
MI ss
- left sided chest pain that is crushing, feeling like constriction of chest, burning or discomfort
- pain radiates to arms/back/jaw, not relieved by rest or nitrogylcerin
- irregular heartbeat, dyspnea, diaphoresis
- denial, severe anxiety, impending doom
MI prognosis
- 65% of deaths occur in first hour
- immediately defibrillation for ventricular fibrillation
- late mortality depend son extent of damage to muscle –> most common cause is fatal arrhythmia
MI etiology
- occlusion of coronary artery resulting in ischemia and infarct of myocardium
- results form insufficient o2 supply
- pain caused by ischemia and if ischemia is not resolved in 6 hours, cardiac muscle dies
- coronary thrombosis is most common cause
MI diagnosis
- thorough history and physicla
- ECG change in PR and QRS complexes correspond to ischemic area
- chest radiography
- lab tests for cardia enzymes
MI treatment
- O2 administration
- morphine for pain
- aspirin to reduce additional damage by ischemia
- basil dilation
- thrombolytic drugs
- angioplasty
MI prevention
lifestyle modification
cardia arrest
sudden, unexpected cessation of cardia activity
cardia arrest ss
- unresponsive
- no respiratory effort or pulse
cardia arrest etiology
- caused by anoxia (absence of o2) or interruption of electrical stimuli to heart
- can be due to respiratory arrest, arrhythmia, MI, electrocution, drowning, severe trauma, hemorrhage, drug overdose
cardiac arrest prognosis
- varies depending on time patient has been in cardia arrest
- earlier CPR into fibrillation have greater possibility for survival
- at 4:00 to 6:00 min after cessation of cardia activity, brain cells start to die
- 10 min, brain will die and death is inevitable
cardiac arrest diagnosis
- absence of respiratory effort
- lack of palpable pulse
- ECG showing verticular fibrillation or asystole
cardiac arrest treatment
- CPR initiated within 4-6 min
- AED
- antiarrhythmic drugs
- epinephrine
cardia arrest prevention
- lifestyle modifications to reduce risk
- cannot predict many accidents
- implantation of defibrillators
hypertensive heart disease
- results of chronically elevated pressure throughout vascular system
- most prevalent cardiovascular disorder in the US
- arteriosclerosis, arteriosclerosis, renal disease, anything increasing vascular pressure can cause heart tow work harder as it pumps against increased resistance
essential hypertension (primary)
abnormally high blood pressure
essential hypertension ss
- insidious onset
- few symptoms until permanent damage (headaches, epistaxis, lightheadedness, syncope)
essential hypertension etiology
- more common with old age
- is accompanied with hyperlipidemia, can lead to atherosclerosis
- ideology unknown but many factors contribute –> stress, age, heredity, smoking, obesity, sedentary lifestyle, poor diet, hyperactive
essential hypertension prognosis
- varies and depends on patients response to drug and lifestyle modifications
essentrial hypertension diagnosis
- blood pressure elevation
- systolic > 140 mmhg
- diastolic > 90 mmhg
essential hypertension treatment
- diuretics to reduce blood volume
- ACE inhibitors to produce vasodilation and increase renal blood flow
- basil dilators to dilate vessels
- CCBs to slow hr, dilate vessels
- reduce conduction irritability
- designed to fit each patient
- lifestyle modifications
essential hypertension prevention
- ideology is unknown so cannot be prevented
- alter contributing factors
malignant hypertension
life threatening, sever form of hypertension
malignant hypertension ss
- severe headache
- blurred vision
- dyspena
- sudden onset
malignant hypertension etiology
- unknown but stress is contributing factor
- at risk for cerebral vascular accident (CVA), stroke, irreversible renal damage
malignant hypertension prognosis
depends on person’s response to drugs
malignant hypertension diagnosis
blood pressure elevation
- systolic > 200 mmhg
- diastolic > 120 mmhg
malignant hypertension treatment
- aggressive intervention –> intravenous vasodilators
- monitor blood pressure
- drug therapy may need stop be continued for life
malignant hypertension prevention
- difficult because etiology unknown
- comply with drug therapy and reduce stress
- similar to essential hypertension
congestive heart failure (CHF)
acute or chronic inability of heart to pump enough blood
CHF ss
- insidious onset with patient experiencing gradually increasing dyspnea
- increased heart and respiratory rates, anxiety
- distended neck viens
- edema in ankles
- liver and spleen enlarge and peripheral edema is more prominent with right sided failure
- pulmonary congestion and more pronounced respiratory difficulties with left sided failure
CHF etiology
- underlying condition can compromise pumping action
- common cause is MI
- can be caused by hypertension, cCAD, COPD< cardia valve damage, arrhythmias, cardiomyopathy
CHF prognosis
- varies
- acute: responds well to medical interventions
- chronic: vulnerable to major organ impairment and complications
CHF diagnosis
- through history and physical
- breath sounds diminished
- radiography indicates fluid in lungs
- ECG to discover underlying causes
- echocardiogram to evaluate chamber size, ventricular function, disease of myocardium, valves, cardia structures, pericardium
- cauterization to monitor pressures in circulation
CHF prevention
- education about contributors to cardiac health and control of blood pressure
- early medical intervention
CHF treatment
- reduce workload of heart and increase efficiency
- digitalis preparations to strengthen and slow heartbeat
- ACE inhibitors and arcs to increase blood flow
- diuretics to reduce volume of fluid in body
- basil dilators to reduce vascular pressure
- aldosterone antagonists
- pacemakers, defibrillators, heart transplant
Cor pulmonale
right sided heart disease
- no prevention
Cor pulmonale ss
- dyspnea
- distended neck veins and edema of extremities
- enlarged and tender liver
cor pulmonale etiology
- enlargement of right ventricle as a result of primary lung disease and pulmonary hypertension
- diseased pulmonary blood vessels impair flow of blood which increases workload of right side of heart
- right ventricle hypertrophies and becomes less effective in pumping blood
- can be caused by emphysema, fibrotic pulmonary lesions, pulmonary emboli
- chronic hypoxemia can stimulate production of RBCs which can increase blood viscosity
cor pulmonale prognosis
- depends on patients response to treatment
cor pulmonale diagnosis
- history of pulmonary disease and hypoxia
- radiography and echocardiography to revel pulmonary congestion and right sides heart enlargement
- ECG shows arrhythmias
- elevated RBC count in polycythemia
cor pulmonale treatment
- relieve causative factors in pulmonary system and reduce hypoxemia
- bronchodilators
- supplemental oxygen
- bed rest
- digitalis preparations
- diuretics if edema is present
- anticoagulants to avoid thromboembolism
- phlebotomy if polycthemia is a porblem
- low salt diet
pulmonary edema
fluid shift into extravascular spaces of lungs
pulmonary edema ss
- dyspnea and coughing
- orthopnea
- increased respiratory and heart rates
- bloody, frothy sputum
- blood pressure may fall
- cold and clammy skin
- symptoms often occur at night he patient lies down
pulmonary edema etiology
- caused by left sided heart failure, mitral valve disease, pulmonary embolism, systemic hypertension, arrhythmias, renal failure, head trauma, drug overdose, high altitudes
- excessive fluid accumulates in pulmonary tissue and air spaces of the lungs pulmonary circulation overloaded with excessive volume of blood
pulmonary edema prognosis
- life threatening condition considered to be medical emergency
- depends on severity of pulmonary edema in response to intervention
pulmonary edema diagnosis
- dyspnea, orthonea, brought blood, frothy sputum are indicative
- breath sounds diminished with rails, rhonchi, wheezing
- bags show reduced oxygen saturation, increased CO2 retention, increased bicarbonate, decreased ph
- radiography shows increased opacity of pulmonary tissue, enlarged heart, prominent pulmonary vessels
pulmonary edema treatment
- place patient in fowler’s position (sitting)
- supplemental oxygen
- diuretics to increase fluid excretion
- vasodilators
- beta adrenergic drugs to dilate bronchioles and control bronchial spasms
- severe: mechanical ventilation
pulmonary edema prevention
- controlled by prevention of heart disease and avoidance of risk factors
cardiomyopathy
non-inflammatory disease of cardiac muscle resulting in enlargement of myocardium and ventricular dysfunction
cardiomyopathy ss
symptoms of CHF
cardiomyopathy etiology
- primary cause unknown
- 3 groups:
dilated: results of chronic alcoholism, autoimmune process, viral infection, results in diffuse degeneration of myocardial fibres, followed by decreasing contractile effort
hypertrophic: genetic and idiopathic, left ventricular wall and inter ventricular septa, hypertrophies resulting in small and elongated left ventricle and possible obstruction of aortic valve
restrictive: infiltrative process of heart caused fibrosis and thickening of myocardium
cardiomyopathy prognosis
- medication improved survival rate
- some can be fatal with only option being heart transplantation
- prognosis for restrictive is poor because changes in cardiac muscle are irreversible
cardiomyopathy diagnosis
- thorough history and physical
- radiograph reveals cardiomegaly associated with acrid murmurs
- ECG reveals rate and rhythm abnormalities
- echocardiography and cardiac catheterization can identify type and extent
- biopsy may be required
cardiomyopathy treatment
- determined by type
- dilated: similar to control of CHF, anti arrhythmic drugs, digitalis, anticoagulants, limit activities
- hypertrophic: reduce workload of heart, beta adrenergic blockers, cabs to reduce blood pressure and relax muscle, ACE inhibitors to relax vessels and reduce workload
- restrictive: reduce workload of heart
cardiomyopathy prevention
non specific depending on original underlying cause
pericarditis
acute or chronic inflammation of pericardium, the sac enclosing/protecting the heart
pericarditis ss
- fever, chills, and malaise
- chest pain that fluctuates with inspiration or heatbeat
- dysnpea
- tachycardia
pericarditis ethology
- blood or inflammatory exudate released into pericardial sac resulting in friction and irritation between the layers
- idiopathic or consequences of infection elsewhere in the body
- acute: adhesions formed between pericardium and heart, can cause loss of elasticity, producing a constrictive pericarditis
- chronic: fibrous calcification of visceral membrane, interfering with heart’s ability to contract normally leading to drop in cardia output
pericarditis prognosis
- acute: usually resolves with full recovery
- chronic: extensive adhesions or calcification may necessitate resection of pericardium
pericarditis diagnosis
- identification of causative organism through blood test
- elevated WBC, erythrocyte sedimentation rate, cardia enzyme levels
- change son ECG
- echocardiogram can reveal presence of pericardial fluid and thickened pericardium
- chronic: cardiac catheterization shows elevated pressure in cardia chambers
pericarditis treatment
- manage underlying systemic disease and reduce inflammation and pain
- bed rest, analgesics, antipyretics, naiads, corticosteroids
- infectious: antibiotics, surgical drainage, aspiration
myocarditis
inflammation of muscular walls of heart
myocarditis ss
- palpitations
- fatigue
- dyspnea
- fever
- arrhythmia
- chest tenderness
myocarditis etiology
- damage to myocardium by pathogenic invasion or toxins (ex. viral, alcohol, complication of other diseases, etc.)
- often idiopathic
- can be acute or chronic
- can involve small part of myocardium or be diffuse
- can occur at any age
- may be associated with myocardial infarction
myocarditis diagnosis
- elevated WBC, ESR, cardia enzymes
- radiographs revealing ventricular enlargement
- abnormal ECG
- biopsy confirming inflammation and identify cause
myocarditis treatment
- infection: anti-infective agents
- rest and reduce heart workload
- medication to stabilize arrhythmias
- analgesics and anti-inflammatory drugs
- supplemental O2
myocarditis prevention
- prevention not always possible
- early treatment of infections with complete course of antibiotics can prevent onset
endocarditis
inflammation of lining and valves of heart
endocarditis ss
- vague to pronounced symptoms of infection (fever, chills, night sweats, weakness, anorexia, fatigue)
endocarditis etiology
- usually secondary to infection elsewhere, resulting of pre-existing heart disease, consequences of immunologic reaction
- vegetative growth on cardiac valves that can be released into bloodstream as emboli resulting in infarcts and new places of infection
- lodge in vessel and cause ischemia in heart, lungs, kidney, brain, extremities
- disruption of valves may cause them to be unable to close affectively, disrupt, or obstruct blood flow - produces cardia murmur
- serious obstruction or regurgitation of blood flow affect pumping effectiveness and causes complications
- patients with damaged cardiac valves as a result of rheumatic disease are more prone
endocarditis prognosis
- early diagnosis and treatment with antibiotics usually bring complete recovery
- untreated cases have poor prognosis
endocarditis diagnosis
- CBC may reveal Leukocytosis, elevated ESR
- blood tests can reveal causative organism
- echocardiogram shows valve involvement with vegetations or abscesses
- ECG may indicate arrhythmia or conduction defects
endocarditis treatment
- identify causative organism and administer anti-infective therapy
- antipyretics, anticoagulants
- bed rest
- surgical repair or replacement of damaged cardia valves
endocarditis prevention
- prophylactic antibiotics before dental work, childbirth, invasive, procedures
rheumatic fever
systemic inflammatory and autoimmune disease involving joints and cardiac tissue
rheumatic fever ss
- fever, polyarthritis (joint pain, limited range of motion, edema, redness)
- joint involved include finger, knew, ankle with inflammation transient
- carditis, cardiac murmurs, cardiomegaly, CHF
- weakness, malaise, anorexia, weigh loss
- abdominal pain, rash on trunk
- small nodules on tendon sheets in knees, knuckles, elbows
rheumatic fever etiology
- 1-5 weeks after upper respiratory infection
- follows sore throat caused by group A beta-hemolytic streptococcus - antibodies against bacteria cross rect with normal tissue causing autoimmune disease where antibodies attach bodies own cells and induce inflammation
- antibodies can migrate to endocardium and mitral valve and sometimes aortic valves where vegetations form
- usually in children
rheumatic fever prognosis
good with treatment
rheumatic fever diagnosis
- history of upper respiratory tract infection
- no single diagnostic feature
- presence of carditis and polyarthritis add evidence
- increase in WBC, cardia enzymes, ESR
rheumatic fever treatment
- course of antibiotics for infection
- antipyretics and anti-inflammatory agent for relief of arthritis
- bed rest
rheumatic fever prevention
prophylactic administration of antibiotics for strep throat
rheumatic heart disease
cardiac manifestations that follow rheumatic fever
rheumatic heart disease ss
- CHF causes dyspnea, tachycardia, edema, nonproductive cough, cardiac murmurs
rheumatic heart disease etiology
- acute endocarditis leading to chronic cardiac involvement includes valvular damage
- vegetations cause stenosis of the valves (specifically mitral/aortic)
- after rheumatic fever, vegetations can be enlarged involves may scar, causing stenosis
- frequency is decreasing as a result of diagnosis and aggressive antibiotic treatment
rheumatic heart disease diagnosis
- history of rheumatic fever and cardia murmurs
- echocardiogram shows vegetations or resulting damage on valves
rheumatic heart disease treatment
- reduce stenosis of valves and prevent further damage
- surgery to relieve stenosis or replace valve
- good dental hygiene to prevent gingival infection which could cause further blood borne infection and damage to valves- prophylactic antibiotics before dental procedures
rheumatic heart disease prevention
prophylactic antibiotics for strep throat
valvular heart disease
- acquired or congenital disorder that involves any of four valves of the heart
- can be insufficient or stenosis:
- insufficient: failure valves to close completely allowing blood to be forced back into previous chamber, adds pressure on the chamber and increases heart workload
- stenosis: hardening of cusps of valves that prevents complete opening, impedes blood flow into next chamber
- mitral valve most often involved
- diagnosis requires ECG, radiography, echocardiogram, catheterization
- treatment involves digitalis or quinidine for arrhythmias and antibiotic prophylaxis
mitral stenosis
hardening of cusps of mitral valve that prevent complete and normal opening for passage of blood from the left atrium to the left ventricle
mitral stenosis ss
- exertion dyspnea and fatigue
- cough and palpitations followed by hemoptysis
- severe: cyanosis
- can be insidious or acute
mitral stenosis etiology
- rheumatic heart disease the cause of most cases
- group A beta-hemolytic streptococcus stimulates antibody production and antibodies attach body in autoimmune response
mitral stenosis prognosis
improves with corrective intervention
mitral stenosis diagnosis
- cardiac murmur including a diastolic murmur
- echocardiogram to confirm
mitral stenosis treatment
- limit sodium
- theoretics to reduce workload on heart
- anticoagulants to prevent formation of thrombi
- digoxin to reduce heart rates
- surgical intervention (commissurotomy) to free valve allow blood-flow
- valve replacement is a final option
mitral stenosis prevention
prevent rheumatic fever and subsequent rheumatic heart disease
mitral insufficiency
mitral valve fails to close completely and allows blood from left ventricle to flow back into left atrium
mitral insufficiency ss
- dyspnea and fatigue
- heart murmur
mitral insufficiency etiology
- may fail to close because of scar tissue resulting form inflammation and vegetations (resulting form endocarditis), rheumatic fever, mitral valve prolapse, CAD, MI, cardiac dilation
mitral insufficiency prognosis
- generally good but an lead to CHF
mitral insufficiency diagnosis
- thorough history, especially of sore throat or rheumatic fever
- heart murmur on auscultation
- echocardiogram discloses insufficiency
- ECG, radiography, catheterization to assess cardia status
mitral insufficiency treatment
- bed rest, supplemental oxygen, antibiotics for infection
- severe: surgical repair, replacement of valve
mitral insufficiency prevention
prevent rheumatic fever and resulting scarring of mitral valve
mitral valve prolapse
one or more cusps of mitral valve protrudes back into left atrium during ventricular contraction
mitral valve prolapse ss
- most are asymptomatic
- can experience dizziness, chest pain, dyspnea, fatigue, syncope, anxiety
mitral valve prolapse etiology
- usually benign
- one of the valve cusps do not close completely
- abnormally long or short chord tendinae may be the cause of valves inability to close properly
- regurgitation of blood occurs during left ventricular systole and results in rushing, gurgling cardiac murmur characteristic of prolapse
mitral valve prognosis
good <3
mitral valve diagnosis
- usually discovered during routine exam
- click-murmur syndrome is heart on auscultation
- the good cardiogram reveals failure of valve to close
mitral valve prolapse treatment
- generally not required for asymptomatic patients
- beta blockers for those with anxiety and discomfort
- avoid caffeine, smoking, large meals
mitral valve prolapse prevention
none known
arrhythmias (irregular heartbeats)
any deviation form normal heartbeat, normal sinus rhythm
arrhythmias ss
- palpitations
- tachycardia
- skipped heartbeats
- bradycardia
- syncope
- fatigue
arrhythmias etiology
- interference with conduction system of heart - SA node (pacemaker(, AV node, bundle branches, purkinje fibre
- ischemia and drugs can cause arrhythmias
- heart block occurs when impulses from SA node becomes slow or irregular at or below the AV node
arrhythmias prognosis
depends on type and cause
arrhythmias prevention
- avoid drugs, causative activities
- some have no prevention
arrhythmias diagnosis
- ECG reveals arrhythmias
- echocardiography may conform particular arrhythmia
- holter monitor to capture arrhythmias
arrhythmias treatment
- depends on case
- drug induced resolved with cessation of drug
- anticoagulants to prevent thromboembolism
- supplemental oxygen
- cardiac electric shock to restore normal heart rhythm
- cardiac ablation
- pacemaker is bradycardia
sinus tachycardia
ss: rate > 100 bpm
etiology: rapid impulse originates from SA Node, conduction normal
diagnosis: rapid rate
treatment: beta blockers, calcium channel blockers, may be candidate for ICD
sinus bradycardia
ss: rate < 60 bpm
etiology: slow impulse originates in SA node, conduction norma
diagnosis: slow rate
treatment: atropine
premature atrial contraction
rate depends on underlying rhythm
etiology: irritable atrium, single ectopic beat that arises prematurely, conduction through ventricle norma
diagnosis: irregular heartbeat, diagnosis by ECG
treatment: no treatment necessary, if needed: antiarrhythmic drugs
atrial tachycardia
ss: rate of 150-250 bpm, sudden onset
etiology: irritable atrium, firing at rapid rates, normal contraction
diagnosis: rapid rate with atrial and ventricular rates identical, diagnosis by ECG
treatment: reflex vagal stimulation, calcium channel-blocking drubs, cardioversion, may be candidate for ICD or ablation
atrial fibrillation
ss: artrial rate > 350 bpm, ventricular rate < 100 bpm (controlled) or > 100 bpm (rapid ventricular response)
etiology: atrial ectopic foci discharging at too rapid and chaotic rate for muscles to respond and contract, resulting in quivering of atrium; AV node blocks some impulses and ventricle response irregular
diagnosis: ECG shows no P waves, grossly irregular ventricular rate
treatment: IV verapamil, if unsuccessful procainamids, if unsuccessful cardioversion, may be candidate for ICD or ablation
first-degree heart block
ss: rate depends on rate of underlying rhythm
etiology: delay at AV node, impulse eventually conducted
diagnosis: ECG shows P-R intervals > 0.2 seconds
treatment: atropine; if unsuccessful, artificial pacemaker insertion
second-degree heart block
ss: intermittent block with progressively longer delay in conduction until one beat is blocked; atrial rate normal, ventricular rate slower than normal, rhythm irrgegular
etiology: SA node initiates impulse, conduction through AV node is blocked intermittently
diagnosis: ECG shows normal P waves, some P waves not followed by QRS complex, P-R interval progressively longer, followed by block of impulse
treatment: mild forms, no treatment; severe, insertion of artificial pacemaker
classic second-degree heart block
ss: ventricular rate slow rhythm, regular; P waves normal, QRS complex dropped every second, third or fourth beat
etiology: SA node initiates impulse, conduction through AV node is blocked
diagnosis: ECG shows P waves present, QRS complex blocked every second, third, or fourth impulse
treatment: artificial pacemaker
third-degree heart block
ss: atril rate normla, ventricular rate 20-40 or 40-60 bpm, no relationship between P wave and QRS complex
etiology: SA node initiates impulse, which is completely blocked from conduction, causing atria and ventricles to beat independently
diagnosis: ECG p waves and QRS complexes with no relationship to each other, rhythms are regular but independent of each other
treatment: artificial pacemaker is necessary
premature ventricular contraction (single focus)
ss: single ectopic beat, arising from ventricle, followed by compensatory paus
etiology: ectopic beat originates in irritable ventricle
diagnosis: ECG shows a wide, bizarre QRS complex > 0,12 second usually followed by compensatory paus
treatment: usually no treatment if <6/min and single focus; may be candidate for ICD or ablation
multifocal arrhythmia
ss: rate dependent on underlying rhythm; rhythm regular or irregular; P wave absent before ectopic beat
etiology:ectopic beat originates in irritable ventricle
diagnosis: ECG shows a wide, bizarre QRS complex (same as single focus)
diagnosis: ECG shows a wide, bizarre QRS complex > 0,12 second usually followed by compensatory pause (same as single focus)
treatment: may be candidate for ICD or ablation
ventricular tachycardia
ss: rate of 150-250 bpm, rhythm usually regular; focus of pacemakers normally single, patient experiences palpitations, dyspnea, and anxiety followed by chest pain
etiology: 4 or more consecutive PVCs at a rapid rate due to advanced irritability of myocardium, indicating ventricular command of heart rate
diagnosis: ECG shows runs of four or more PVCs, P wave buried in QRS complex
treatment: immediate intervention necessary - IV lidocaine if unsuccessful, follow by cardioversionl procainamide or bretylium may be used this is a candidate for ICD or ablation
ventricular fibrillation (lethal arrhythmia)
ss: patient loses consciousness immediately after onset no peripheral pulses palpable, no heart sounds; no blood pressure
etiology: ventricular fibers twitch rather than contract, reason unknown
diagnosis; pulseless, unconsciousness patient ECG shows rapped, predictive, chaotic waves originating in ventricle
treatment: recognize and terminate rhythm; precordial shock (defibrillation); survivors become candidates for ICD and ablation
shock
collapse of cardiovascular system
shock ss
- vasodilation and fluid shift
- inefficient cardia output
- pale, cold, clammy skin
- rapid, weak, thready pulse
- rapid bretahing
- altered level of consciousness, anxiety, irritability, restlessness, impending doom
- blood pressure drops
- dizziness, thirst, sweating
- late stages: dilation of pupils, dull nd lustreless eyes, shaking, trembling
shock etiology
- inadequate perfusion of organs and tissues
- can be caused anaphylaxis, hemorrhage, sepsis, respiratory distress, heart failure, neurologic failure, emotional catastrophe, severe metabolic insult, failure of heart to pump adequately, inadequate oxygen, vascular collapse with massive dilation causing blood to pool away from vital area
- reduction of blood circulating the body o that vital organs do not receive enough blood and nutrients
shock prognosis
- intermediate assessment and intervention improves prognosis for complete or near complete recovery
- can become unstoppable and irreversible if not addressed
shock diagnosis
thorough history and physical
shock treatment
- immediate intervention needed to halt progression
- maintain open airway and established ventilation
- control bleeding, surgery for internal
- supine position with legs and feet elevated
- keep warm
- volume replacement if needed
shock prevention
- most occurrences bot preventable
- immediate intervention prevents rapid progression condition into a fatal occurrence
cardiogenic shock
inadequate output of blood by the heart
cardiogenic shock ss
- experienced symptoms of shock
- hypertensive state that continues to worsen
cadriogenic shock etiology
- myocardium fails to pump effectively
- usually preceded by MI, severe heart failure, arrhythmias, acute valve failure
cardiogenic shock prognosis
- varies but is mostly unfavourable
- immediate assessment and intervention
cardiogenic shock diagnosis
- thorough history and physical
- ECG, radiography
cardiogenic shock treatment
- general measures for shock
- medications that increase efficiency of myocardium
- can insert intra-aortic ballon pump
caridogenic shock prevention
prevention unlikely
cardiac tamponade (cardiac compression)
compression of heart and muscle and restriction of heart movement caused by blood or fluid trapped in pericardial sac
cardiac tamponade ss
- sudden severe dyspnoea and rapid falling blood pressure
- weak thready, rapid pulse
- shock and cyanosis
- loc falls
cardiac tamponade etiology
- coronary epicardial, pericardial vessel breaks and blood is trapped in pericardial sac
- myocardium may rupture
- restricts heart movement so less blood can enter
- can result form insult integrity of vessel
- pressure of blood causes heart to beat inappropriately leading to cardia arrest
- can occur in people with cancer, chronic kidney failure, hypthyrooidism, upus
cardiac tamponade prognosis
- varies and depends on causative factors, successive intervention, health status
- surgical repair usually has positive outcome
cardiac tamponade diagnosis
- through history and physical
- muffled or distant heart sounds
- breath sounds normal
cardiac tamponade treatment
- insert needle into pericardial space and withdraw offending blood
- surgery to repaire leak
cardiac tamponade prevention
not possible
anemia
- condition of abnormally low # of RBC that leads to reduced deliver of O2 and nutrients
- causes hemorrhage, excessive destruction of RBCs, nutritional deficient, and chronic disease
- ss: fatigue, decreased tolerance for exercise, weakness, shortness of breath, etc.
disorders of hemostasis
- commonly knows as bleeding disorders
- includes a range of medical problems that lead to poor blood clotting and continuous bleeding
- can result from abnormal platelet function/#, vitamin K deficiency, or clotting factor deficiencies
- purpura: inflammation of blood vessels that cause red splotches over body
age-related diseases
- anemia is most common blood disorder in people over 75
- causes of this disease include blood loss, nutrition deficiencies, chronic illness, and chronic renal failure
- ss: decreased physical activity, mental states changes, an increase in mortality
